Dyslipidaemia: Current Therapy and Future Prospectus
Journal Title: Scholars Journal of Applied Medical Sciences - Year 2015, Vol 3, Issue 3
Abstract
: Dyslipidaemia is a major cause of atherosclerosis and atherosclerosis-induced conditions, such as coronary heart disease (CHD), ischemic cerebrovascular disease and peripheral vascular disease. These conditions cause morbidity or mortality in a majority of middle-aged or older adults and account for about one-third of all deaths of persons in this age range. The incidence and absolute numbers will likely increase over the next decade because of the epidemic of obesity and the aging of the population. When pharmacotherpy is indicated, providers can choose from multiple agents with proven efficacy i.e. statins are the first-line drugs for treatment of dyslipidemia, but they do not address all CVD risk. Recognition that dyslipidemia is a risk factor has led to the development of drugs that modify cholesterol levels. The ongoing development of novel therapies include (i) Low-density-lipoprotein (LDL) cholesterol concentrations reduction by the use of antibodies to proprotein convertase subtilisin/kexin-9, antisense oligonucleotide inhibitors of apolipoprotein B production, acyl-coenzyme A cholesterol acyl transferase inhibitors and microsomal transfer protein (MTP) inhibitors; (ii) Triglyceride-rich lipoproteins level reduction with ω-3 fatty acids, inhibitors of MTP and diacylglycerol acyl transferase-1; and (iii) increase the level of high-density-lipoprotein (HDL) cholesterol levels, HDL particle numbers, and/or HDL functionality using cholesteryl ester transfer protein inhibitors, agents derived from HDL, apolipoprotein AI mimetic peptides, and microRNAs. This review article focuses on the currently available hypolipdemic drugs, their limitation and novel strategies for treatment of dyslipidaemia. Keywords: Dyslipidaemia, Lipoprotein, Statins, CETP inhibitor, PCSK-9 inhibitor.
Authors and Affiliations
Rajendra Sharma, D C Dhasmana, Taruna Sharma, Juhi Kalra
Keywords
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